Cav-1 Ablation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Growth through Nrf2-Induced shh Signaling
Joint Authors
Li, Xuqi
Li, Wei
Lei, Jianjun
Wang, Zheng
Shao, Shan
Qin, Tao
Qian, Weikun
Han, Liang
Zhang, Dong
Ma, Qingyong
Wu, Zheng
Wu, Erxi
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-04-20
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
A more comprehensive understanding of the complexity of pancreatic cancer pathobiology, especially, and understanding of the role of the tumor microenvironment (TME) in disease progression should pave the way for therapies to improve patient response rates.
Previous studies reported that caveolin-1 (Cav-1) has both tumor-promoting and tumor-suppressive functions.
However, the function of Cav-1 in the pancreatic cancer microenvironment remains largely unexplored.
Here, we show that coinjection of Cav-1-silenced pancreatic stellate cells (PSCs) with pancreatic cancer cells increased tumor growth.
To comprehensively characterize paracrine communication between pancreatic cancer cells and PSCs, PSCs were cultured with pancreatic cancer cell conditioned medium (CM) containing cytokines.
We reveal that Cav-1-silenced PSCs facilitated the growth of pancreatic cancer cells via enhanced paracrine shh/MMP2/bFGF/IL-6 signaling.
Specifically, Cav-1-silenced PSCs exhibited increased shh expression, which heterotypically activated the shh signaling pathway in pancreatic cancer cells.
Moreover, Cav-1-deficient PSCs accumulated ROS to enhance the shh pathway and angiogenesis in pancreatic cancer cells.
In addition, overexpression of Nrf2 reversed the effects of Cav-1 knockdown on PSCs, increasing ROS production and enhancing paracrine shh/MMP2/bFGF/IL-6 signaling.
Together, our findings show that stromal Cav-1 may mediate different mechanisms in the complex interaction between cancer cells and their microenvironment though Nrf2-induced shh signaling activation during pancreatic cancer progression.
American Psychological Association (APA)
Shao, Shan& Qin, Tao& Qian, Weikun& Li, Xuqi& Li, Wei& Han, Liang…[et al.]. 2020. Cav-1 Ablation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Growth through Nrf2-Induced shh Signaling. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1203842
Modern Language Association (MLA)
Shao, Shan…[et al.]. Cav-1 Ablation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Growth through Nrf2-Induced shh Signaling. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1203842
American Medical Association (AMA)
Shao, Shan& Qin, Tao& Qian, Weikun& Li, Xuqi& Li, Wei& Han, Liang…[et al.]. Cav-1 Ablation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Growth through Nrf2-Induced shh Signaling. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1203842
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203842